Tissue Doppler echocardiography for evaluation of patients with ventricular resynchronization therapy.

INTRODUCTION AND OBJECTIVE

Ventricular resynchronization therapy optimizes cardiac function and induces reverse remodeling of the left ventricle (LV) in patients (pts) with dilated cardiomyopathy and intraventricular conduction disturbances. Improvement of LV mechanical synchrony seems to be the predominant mechanism. There is a growing interest in objective quantification of desynchronization. This study aims to evaluate the effect of ventricular resynchronization therapy on LV remodeling and on LV desynchronization, assessed by tissue Doppler echocardiography.

PATIENTS

We studied ten pts, eight male, mean age 65 +/- 10 years, with dilated cardiomyopathy, intraventricular conduction disturbances and heart failure, New York Heart Association functional class III or IV. Five pts had coronary artery disease and the others idiopathic dilated cardiomyopathy. All pts had an implanted cardioverter, defibrillator with cardiac resynchronization therapy. The LV pacing electrode was placed in the lateral or posterolateral vein.

METHODS

Before and one month after resynchronization therapy the following parameters were measured with conventional Doppler echocardiography: LV end-diastolic (LVd) and end-systolic (LVs) size, ejection fraction (EF) and mitral regurgitation (MR) area. For diastolic function the maximum velocity of the E wave (MV-E) and A wave (MV-A), E/A ratio, LV filling time (LV-FT) and isovolumetric relaxation time (IVRT) were meadured. Mitral longitudinal motion was studied with pulsed tissue Doppler. Maximum velocity of the systolic S wave (MV-S) and isovolumetric contraction time (IVCT) were measured in the tissue Doppler curve of the septum and lateral, inferior and anterior walls. To evaluate the degree of desynchronization the RV index was calculated for each patient, based on the difference between the maximum and minimum IVCT, normalized for the maximum IVCT.

RESULTS

There was a significant reduction in LVd and MR. EF increased significantly (p = 0.003). There were no differences in diastolic function parameters. MV-S did not increase significantly. IVCT increased significantly at the lateral wall (p = 0.037). The RV index demonstrated a significant reduction in ventricular desynchronization (p = 0.001).

CONCLUSIONS

Ventricular resynchronization therapy induces reverse remodeling and improves LV function in selected pts. Improvement of mechanical LV synchrony seems to be the predominant mechanism. Ventricular desynchronization can be measured by tissue Doppler echocardiography.